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Regulatory T (Treg) cells in cancer: can Treg cells be a new therapeutic target?

Cancer Science 2019 May 19
Regulatory T (Treg) cells suppress abnormal/excessive immune responses to self- and non-self-antigens to maintain immune homeostasis. In tumor immunity, Treg cells are involved in tumor development and progression by inhibiting anti-tumor immunity. There are several Treg-cell immune suppressive mechanisms: inhibition of co-stimulatory signals via CD80 and CD86 expressed by dendritic cells through CTLA-4, IL-2 consumption via high-affinity IL-2 receptors with high CD25 (IL-2 receptor ∝ chain) expression, secretion of inhibitory cytokines, metabolic modulation of tryptophan and adenosine, and direct killing of effector T cells. Treg-cell infiltration into the tumor microenvironment (TME) occurs in multiple murine and human tumors. Treg cells are chemoattracted to the TME via chemokine gradients such as CCR4-CCL17/22, CCR8-CCL1, CCR10-CCL28, and CXCR3-CXCL9/10/11. Treg cells are then activated and inhibit anti-tumor immune responses. A high infiltration by Treg cells is associated with poor survival in various types of cancer. Therefore, strategies to deplete Treg cells and control of Treg-cell functions to increase anti-tumor immune responses are urgently required in the cancer immunotherapy field. Various molecules that are highly expressed by Treg cells, such as immune checkpoint molecules, chemokine receptors, and metabolites, have been targeted by antibodies or small molecules, but additional strategies are needed to fine-tune and optimize for augmenting anti-tumor effects restricted in the TME while avoiding systemic autoimmunity. Here, we provide a brief synopsis of these cells in cancer and how they can be controlled to achieve therapeutic outcomes.

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